Evidence map›Paper›PMID 25009785›Full record

ReviewRedox biology2014

Concerted action of Nrf2-ARE pathway, MRN complex, HMGB1 and inflammatory cytokines - implication in modification of radiation damage.

Anuranjani, Madhu Bala

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.7field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

67 citing papers in PubMed, 135 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Heliyon · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Roles of NRF2 in DNA damage repair.Cellular oncology (Dordrecht, Netherlands) · 2023
    Review
  15. Review
  16. Article
  17. Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023
    Review
  18. Review
  19. Article
  20. Review

7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

AnuranjaniRadiation Biology Department, Institute of Nuclear Medicine and Allied Sciences, Brig SK Mazumdar Marg, Delhi -110054, India.
Madhu BalaRadiation Biology Department, Institute of Nuclear Medicine and Allied Sciences, Brig SK Mazumdar Marg, Delhi -110054, India.
Institute of Nuclear Medicine & Allied Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Whole body exposure to low linear energy transfer (LET) ionizing radiations (IRs) damages vital intracellular bio-molecules leading to multiple cellular and tissue injuries as well as pathophysiologies such as inflammation, immunosuppression etc. Nearly 70% of damage is caused indirectly by radiolysis of intracellular water leading to formation of reactive oxygen species (ROS) and free radicals and producing a state of oxidative stress. The damage is also caused by direct ionization of biomolecules. The type of radiation injuries is dependent on the absorbed radiation dose. Sub-lethal IR dose produces more of DNA base damages, whereas higher doses produce more DNA single strand break (SSBs), and double strand breaks (DSBs). The Nrf2-ARE pathway is an important oxidative stress regulating pathway. The DNA DSBs repair regulated by MRN complex, immunomodulation and inflammation regulated by HMGB1 and various types of cytokines are some of the key pathways which interact with each other in a complex manner and modify the radiation response. Because the majority of radiation damage is via oxidative stress, it is essential to gain in depth understanding of the mechanisms of Nrf2-ARE pathway and understand its interactions with MRN complex, HMGB1 and cytokines to increase our understanding on the radiation responses. Such information is of tremendous help in development of medical radiation countermeasures, radioprotective drugs and therapeutics. Till date no approved and safe countermeasure is available for human use. This study reviews the Nrf2-ARE pathway and its crosstalk with MRN-complex, HMGB1 and cytokines (TNF-a, IL-6, IFN-? etc.). An attempt is also made to review the modification of some of these pathways in presence of selected antioxidant radioprotective compounds or herbal extracts.

Indexed as

Antioxidant Response ElementsCell Cycle ProteinsCytokinesDNA-Binding ProteinsDNA DamageDNA RepairDNA Repair EnzymesHMGB1 ProteinHumansNF-E2-Related Factor 2Signal TransductionCell Cycle ProteinsCytokinesDNA-Binding ProteinsDNA Repair EnzymesHMGB1 ProteinNF-E2-Related Factor 2AP1, activator protein-1ARE, antioxidant response elementATM, ataxia telangiectasia mutagenesisBcl-2, B cell lymphoma-2 proteinbFGF, basal fibroblast growth factorCBP, CREB-binding proteinChk-2, checkpoint kinase-2 proteinDAMP, death associated molecular patternDDR, DNA damage responseDGR, double glycine repeatsDSB, double strands breakFGF2, fibroblast growth factor-2FGF, fibroblast growth factorGM-CSF, granulocytes macrophages colony stimulating factorGPx, glutathione peroxidaseGSH, glutathione (reduced)GSK-3ß, glycogen synthase kinase 3 betaHMGB1HMGB1, high mobility group Box 1HR, homologous recombinationIR, ionizing radiationKeap1, Kelch like ECH associated protein 1LET, linear energy transferMDA, malondialdehydeMIP, macrophages inflammatory proteinsMRN complexMRN, Mre11, Rad50 and Nbs1 subunitsMRP, multidrug resistance proteinNADPH, nicotinamide adenine dinucleotide phosphateNES, nuclear export sequenceNHEJ, non-homologous end joiningNLS, nuclear localization sequenceNrf2-ARE pathway.OH, hydroxyl radicalPKC, protein kinase CRadio-modificationRAGE, receptor for advance glycation end productsRIF, radiation induced fociRNS, reactive nitrogen speciesROS, reactive oxygen speciesSOD, superoxide dismutaseSSBs, single strand DNA breakst-BHQ, tert butyl hydroquinoneTRAIL, TNF related apoptosis inducing ligandTWEAKTWEAK, tumour necrosis factor weak inducer of apoptosisVEGF, vascular endothelial growth factorVSMC, vascular smooth muscle cells

Identifiers

PMID25009785
PMCPMC4085347
OpenAlexW2093640633

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.